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首页> 美国卫生研究院文献>Infection and Immunity >Presence of a macrophage-mediated suppressor cell mechanism during cell-mediated immune response in experimental visceral leishmaniasis.
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Presence of a macrophage-mediated suppressor cell mechanism during cell-mediated immune response in experimental visceral leishmaniasis.

机译：在实验性内脏利什曼病的细胞介导的免疫反应过程中巨噬细胞介导的抑制细胞机制的存在。

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In susceptible BALB/c mice, systemic intracellular infection with Leishmania donovani provokes generation of adherent spleen cells which can suppress both mitogen- and specific-antigen-stimulated T-cell responses. To characterize the responsible suppressor cell, we irradiated (2,000 R) adherent spleen cells from L. donovani-infected mice or treated them with anti-Thy-1.2 antibody plus complement. Neither anti-T-cell treatment diminished the capacity to inhibit lymphocyte proliferative activity. In addition, as judged by morphologic and functional criteria, 80 to 90% of the adherent cells appeared to be macrophages. Four observations suggested an immunopathogenic role for these suppressor macrophages. (i) Their appearance and disappearance paralleled the establishment and resolution of L. donovani visceral infection in vivo. (ii) Suppressive effects included inhibition of production of the macrophage-activating lymphokine gamma interferon (IFN-gamma). (iii) On transfer into immune mice, suppressor macrophages impaired naturally acquired resistance to L. donovani. (iv) Inhibition of macrophage prostaglandin metabolism by indomethacin reduced suppressor activity in vitro and resulted in a 50% decrease in parasite visceral replication in vivo. In addition, prophylactic cyclophosphamide treatment inhibited the development of suppressor macrophages, and under these conditions visceral infection was rapidly controlled. These results suggested that disseminated L. donovani infection provokes a macrophage-mediated suppressor mechanism which appears to contribute to establishment of visceral leishmaniasis in a susceptible host.
机译：在易感的BALB / c小鼠中，多形性利什曼原虫的全身细胞内感染引起粘附脾细胞的生成，该粘附细胞可以抑制促分裂原和特异抗原刺激的T细胞反应。为了表征负责任的抑制细胞，我们辐照了（2,000 R）感染了多诺威尼酵母的小鼠的脾脏细胞，或用抗Thy-1.2抗体加补体对其进行了处理。两种抗T细胞治疗均未减弱抑制淋巴细胞增殖活性的能力。此外，根据形态和功能标准判断，80-90％的粘附细胞似乎是巨噬细胞。四个观察结果提示这些抑制性巨噬细胞具有免疫致病作用。 （i）它们的出现和消失与体内多诺氏乳杆菌内脏感染的建立和消退相似。 （ii）抑制作用包括抑制巨噬细胞活化的淋巴因子γ干扰素（IFN-γ）的产生。 （iii）抑制巨噬细胞转移到免疫小鼠中后，自然削弱了其对多诺氏乳杆菌的抗性。 （iv）吲哚美辛抑制巨噬细胞前列腺素的代谢降低了体外抑制活性，并导致体内寄生虫内脏复制降低了50％。另外，预防性环磷酰胺治疗抑制了抑制性巨噬细胞的发育，并且在这些条件下内脏感染得到了快速控制。这些结果表明，散发的多诺氏乳杆菌感染引起了巨噬细胞介导的抑制机制，该机制似乎有助于在易感宿主中建立内脏利什曼病。

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